Increased membraneous calcium concentrations in primary hypertension: a causal link to pathogenesis?

Citation
M. Kosch et al., Increased membraneous calcium concentrations in primary hypertension: a causal link to pathogenesis?, J HUM HYPER, 15(1), 2001, pp. 37-40
Citations number
19
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF HUMAN HYPERTENSION
ISSN journal
09509240 → ACNP
Volume
15
Issue
1
Year of publication
2001
Pages
37 - 40
Database
ISI
SICI code
0950-9240(200101)15:1<37:IMCCIP>2.0.ZU;2-B
Abstract
Background: Disturbance in calcium metabolism has been suggested in the pat hogenesis of hypertension, however, membrane calcium content in humans has not been studied in detail yet in primary hypertension. We compared plasma, intracellular and membrane calcium concentrations in erythrocytes of patie nts with essential hypertension and in healthy, normotensive control subjec ts to determine a possible alteration of membrane calcium in primary hypert ension. Subjects and Methods: Thirty-four never treated patients with essential hyp ertension were included and 34 healthy, age- and sex-matched volunteers ser ved as controls. Atomic absorption spectroscopy was used for measurement of intracellular and membrane calcium content in erythrocytes and plasmalemma l preparations. Results: Plasma and intracellular Ca++ concentrations were not significantl y different between hypertensives and controls (plasma: 2.59 +/- 0.18 vs 2. 50 +/- 0.16 mmol/l, intracellular: 1.89 +/- 0.20 mmol/l vs 1.97 +/- 0.24 mm ol/l, NS resp,, mean +/- s.e.m.). However, membrane calcium content was sig nificantly higher in hypertensive patients compared to control subjects (2. 38 +/- 0.28 mu mol/g membraneous protein vs 0.86 +/- 0.32 mu mol/g membrane protein, P < 0.01). Membrane calcium content was correlated to mean arteri al blood pressure (r = 0.59, P < 0.01). Conclusion: Membrane calcium content is significantly increased in patients with untreated primary hypertension and correlates to blood pressure level s. This data suggest, that an membrane mechanism may contribute to alterati ons in calcium metabolism and to the pathogenesis of primary hypertension.